| Pulsatile tinnitus (PT) is not a rare symptom in clinical otology, the persistence ofwhich may cause decreasing of the life quality severely, and even depression and suicide.The key point for tinnitus therapy is to identify the etiologies, which may be mainlycomposed of arterial, venous and neoplastic ones. The venous etiologies have beenincreasingly reported recently, of which the sigmoid dehiscence has been verified as onecommon and curable cause of PT. In last4years,1032patients with PT were performedwith dual enhanced CT (DECT),44%of who were found with sigmoid dehiscence.However, the symptom in40%of85patients with surgical reconstruction was notalleviated after surgical reconstruction. Furthermore, other effective treatments are stilllacking. The key point is that the pathogenesis for dehiscent sigmoid plate tinnitus (DSPT)is still unknown. Until now, the study about DSPT are rarely reported, most of which wereabout surgical description with small samples. The characteristics of DSPT have not yetbeen systematically evaluated. The mechanism of DSPT has not been investigated. Thus,the purpose of this study aims to evaluate the characteristics of DSPT and to establish thestandardized evaluation using CT. Then, to further investigate DSPT’s possible mechanismusing skull model. This study was divided into two parts. Part1, to establish a standardizedassessment of DSPT using CT in order to help surgical positioning; to assess the associatedsigns of DSPT for the further investigation of its mechanism. Part2, to make the skullmodel of DSPT based on the results of part1so as to assess the possible mechanism as thebasis of new treatment options.Part1The CT Study of Dehiscent Sigmoid Plate TinnitusPurpose: To assess the CT characteristics of dehiscent sigmoid plate tinnitus (DSPT) andto establish a standardized assessment.Material and Methods: The DECT images of30patients with unilateral PT cured bysurgical reconstruction were reviewed. Meanwhile,30patients meeting our inclusioncriteria were enrolled as the control group, all of whom were performed with CTangiography reconstructed with both standardized and bone algorithm. The presence of thedehiscence itself (location, extent, amount) and its concomitant signs (the high jugular bulb,the amount and size of emissary veins, the height of pituitary and hypophysial fossa, temporal bone pneumatization, venous outflow dominance, transverse sinus stenosis,arachnoid granulation beneath transverse sinus) were comprehensively analysed by twoexperienced neuroradiologists respectively.Results: Forty-four portions of dehiscence were found in these30patients,17of whomwith single defect. The sigmoid wall was divided into three vertical parts and the superiorportion was mostly involved (29portions). Meanwhile, the sigmoid wall was also dividedinto three horizontal parts (lateral, anterior and posterior walls) and the lateral wall wasmostly involved (40portions). The dehiscence mostly located posterior-superiorly to themastoid tip and the middle point of external canal. The coordinate point was (-3.82,31.58)mm,(-18.37,12.19) mm respectively. The mean transverse diameter of the dehiscence was(2.83±1.29) mm and the mean area was (7.97±5.17) mm. Besides, single defect on thecontra-lateral side was also found in3patients, in whom the mean diameter and area were1.9mm and3.7mm2respectively.Compared with patients in the control group, the presences of high jugular bulb (28vs19), ipsilaterl (25vs6), contralateral (30vs9) and bilateral (25vs5) transverse sinusstenosis, ipsilateral venous outflow dominance (22vs8) were more common; the heightsof pituitary were less ((10.04±2.70) mm vs (8.61±2.70) mm); the heights of pituitary fossawere larger ((10.04±2.70) mm vs (8.61±2.70) mm). However, there were no difference inthe presences of mastoid emissary vein (21vs21), petrosqumousal sinus (2vs1), diploicvein (20vs20), the skull impression caused by arachnoid granulation (18vs18) and thedegree of temporal bone pneumatization ((3.70±1.81) ml vs (4.10±1.81) ml).Eleven patients were rechecked with DECT,6of who were found with incompletesigmoid wall with the mean remnant area of1.9mm2. The dural sinuses were found with noobvious changing compared with preoperative one. The remnant volume of temporal bonepneumatization was2.69ml, which was smaller than that of pre-operation.Conclusion: The dehiscence in patients with DSPT is characterized by one or more defectsof sigmoid plate, mostly with the lateral wall and superior portion involved. The extentsare usually small and irregular. The reference points are beneficial for intra-operativelocation. The hemodynamic abnormalities caused by diversified factors may be the rootcause of DSPT; the associated factors include ipsilateral venous outflow dominance, possible intracranial hypertension, transverse sinus stenosis, high jugular bulb and so on.The dehiscent sigmoid plate with considerable extent may be the key point why the DSPTmay be received. The degree of temporal bone pneumatization is similar to that in normalpeople. Part2The Mechanism Study of Dehiscent Sigmoid Plate Tinnituspurpose: To establish the skull model of dehiscent sigmoid plate tinnitus (DSPT) in orderto investigate its mechanism.Material and Methods: Twenty-two temporal bones were performed using CT. All imageswere reconstructed by Mimics and Geomagic software to make the3D morphology ofsigmoid sinuses, which were printed into real3D entocoele. Then, thin-walled3D artificialvessels were obtained by sprinkling of chemical materials, shaping, cooling and departing.The venous blood was estimated by water and60%glycerol separately. A small andvoiceless water pump was modeled as a heart pumping. A subtle vibratory/acoustic signalreceiver was respectively used to receive the vibration/noise made by water flowing. TheLabview2012software was used to display vibratory/acoustic signal. The temporal boneswere contained by paraffin wax.The sigmoid plate model was made to investigate the role of sigmoid wall dehiscencein vibration/noise transmitting. The temporal bone pneumatization models were made toinvestigate the role of pneumatizated degree in vibration/noise transmitting. Then,completed DSPT model were made based on these two models. The role of hemodynamicabnormalities in DSPT was evaluated through adjusting the flow rate and adjacent canaldiameter respectively. The role of sigmoid wall dehiscence was further evaluated throughchanging its extent. The role of different mediators was also investigated.Results: The flow noise can not be detected by the vibration/noise receiver when thesigmoid plate was intact while obvious noise can be received by noise receiver only whena2mm focal defect was made in the superior segment of sigmoid plate by bone drill. Intwo temporal bones with different degree of pneumatization (2.6ml vs5.2ml), the noisewas larger in the less pneumatizated one. The noise became larger as the extent of dehiscence was increased but without a linear changing. The noise was larger with the flowrate of20ml/s than that of12m/s. The noise was larger in model with stenosis of caliberadjacent to the dehiscence than that without stenosis. Besides, the noise was larger madeby the flow of water than that of glycerol.Conclusion: The hemodynamic state is the root cause of DSPT. The sigmoid walldehiscence is the key factor of DSPT received by inner ear. The degree of the noise wasaffected by both blood flow state and the extent of dehiscence. Surprisingly, the degree ofthe noise has a negative relevance with the degree of temporal bone pneumatization. |
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